Y2, the Smallest of the Sendai Virus C Proteins, Is Fully Capable of both Counteracting the Antiviral Action of Interferons and Inhibiting Viral RNA Synthesis

doi:10.1128/JVI.75.8.3802-3810.2001

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Journal of Virology, April 2001, p. 3802-3810, Vol. 75, No. 8
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.8.3802-3810.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Y2, the Smallest of the Sendai Virus C Proteins, Is Fully Capable of both Counteracting the Antiviral Action of Interferons and Inhibiting Viral RNA Synthesis

Atsushi Kato,¹^,^* Yukano Ohnishi,² Masayoshi Kohase,¹ Sakura Saito,¹ Masato Tashiro,¹ and Yoshiyuki Nagai³

Department of Viral Diseases and Vaccine Control¹ and AIDS Research Center,³ National Institute of Infectious Diseases, Tokyo 208-0011, and Bio-oriented Technology Research Advancement Institution, Saitama 331-8367,² Japan

Received 3 November 2000/Accepted 10 January 2001

An open reading frame (ORF) overlapping the amino-terminal portion of the Sendai virus (SeV) P ORF in the +1 frame producesa nested set of carboxy-coterminal proteins, C', C, Y1, and Y2,which are referred to collectively as the C proteins. The C proteinsare extremely versatile triple-role players; they counteract theantiviral action of interferons (IFNs), inhibit viral RNA synthesis,and are involved in virus assembly. In this study, we establishedHeLa cell lines stably expressing the C, Y1, and Y2 proteins individuallyand examined the capacities of these cells to circumvent the antiviralaction of alpha/beta IFN (IFN- $alpha$ / $beta$ ) and IFN- $gamma$ and to inhibit viraltranscription. The assay protocols included monitoring of IFN- $alpha$ / $beta$ -mediatedsignaling by interferon-stimulated response element-driven reportergene expression and of the antiviral state induced by IFN- $alpha$ / $beta$ and IFN- $gamma$ and measurement of reporter gene expression from anSeV minigenome, as well as quantification of SeV primary transcripts.When necessary, the activities measured were carefully normalizedto the expression levels of the respective C proteins in cells.The data obtained clearly indicate that the smallest protein,Y2, was as active as the C and Y1 proteins in both counteractingthe antiviral action of IFNs and inhibiting viral transcription.The data further show that intracellular transexpression of eitherC, Y1, or Y2 rendered HeLa cells moderately or only poorly permissivefor not only wild-type SeV but also 4C( $-$ ) SeV, which expressednone of the four C proteins. On the basis of these findings, theroles of SeV C proteins in the natural life cycle arediscussed.

^* Corresponding author. Mailing address: Department of Viral Diseases and Vaccine Control, National Institute of InfectiousDiseases, Gakuen 4-6-7, Musahi-Murayama, Tokyo 208-0011, Japan.Phone: 81-42-561-0711, ext. 530. Fax: 81-42-567-5631. E-mail:akato{at}nih.go.jp.

Journal of Virology, April 2001, p. 3802-3810, Vol. 75, No. 8
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.8.3802-3810.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

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